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PIGEON BREEDER’S HYPERSENSITIVITY PNEUMONITIS
– SYMPTOMS INFLUENCED BY STATINS?
C Rooney, K Weir, U Chetty, V Morrison,
A Hood, I Fraser1, M R Adamson, SJ Bourke2, CP McSharry1,
K Anderson. Crosshouse Hospital, Kilmarnock, Department
of Immunology1, University of Glasgow, Scotland, Royal Victoria
Infirmary Newcastle2.
Background
Pigeon breeder’s lung is an immune-driven hypersensitivity
pneumonitis (HP) consisting of granulomatous lesions, lymphocytes,
plasma cells, and lipid laden macrophages. There are early
anecdotal reports of HP patients improving after the introduction
of statin therapy. Previous work from our group (Thorax 2007;
62(suppl 3) A45) has shown significant changes in the serum
lipid profile of pigeon fanciers associated with inflammation
and specific antigen sensitisation which suggests that HP
is a systemic inflammatory illness which may in part be caused
by altered lipid metabolism.
Methods
A questionnaire based prospective assessment of 564 volunteers
at the national pigeon show over a 2 year period (2008 –
2009). Data was collated on exposure, symptoms, diagnostic
investigations, medical history, avian serology and pulmonary
function tests. 119 patients were identified as having pigeon
breeder’s disease as evidenced by clinical symptoms,
imaging or lung biopsy. Smokers, as well as pigeon breeders
with concomitant lung disease were excluded from the analysis.
Comparison of symptom severity, antibody titre and FEV1/FVC
ratio was made between pigeon breeders with HP on and not
on statin treatment. Statistical analysis was carried out
using Levene’s Test on SPSS 16.0.
Results
93 patients were found to meet the inclusion criteria: 25
on statins and 67 without. The average age was 59 years (SD
10). There was no significant difference in FEV1/FVC ratio
(0.69 v 0.77 p=0.67) or antibody titre (43 v 35 p=0.86) between
the statin and non statin cohorts. However the number of symptoms
reported following similar avian exposure in the statin group
was lower (3.8 v 4.5 p=0.04).
Conclusion
Aspects of our study appear to support the hypothesis that
the use of statins can have a palpable clinical impact on
patients with HP. This observation and our previous work suggests
that an interventional statin study would be appropriate.
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